Low-Grade Phyllodes Tumor of the Seminal Vesicle Treated With Laparoscopic Excision

Mohammad Shamim Khan FRCS (Urol) FEBU; Lail-Umah Zaheer MBBS; Kamran Ahmed MBBS; Declan Cahill MSc FRCS (Urol); Catherine Horsefield FRCPath; Giles Rootenberg FRCR; Prokar Dasgupta MD, FRCS (urol) FEBU

Disclosures

Nat Clin Pract Urol. 2007;4(7):395-400. 

In This Article

Discussion of Diagnosis

Primary seminal vesicle tumors are very rare; less than 100 cases have been reported in the English literature to date. Patients usually present with lower urinary tract symptoms or hematospermia. As diagnosis is often delayed, dissemination at presentation is not uncommon. Seminal vesicles are, however, usually involved secondarily to tumors from adjacent organs, particularly the prostate. Tumors of the seminal vesicles can be classified into three groups: primary adenocarinoma; metastases and contiguous spread; soft tissue and other tumors.

Among the primary neoplasms, adenocarcinoma is the most common primary malignant tumor of the seminal vesicles. Mean age at presentation is 62 years (range 17-90 years). The majority of patients present with symptoms of urinary outflow obstruction or hematospermia.[1,2]

As secondary tumors are more common than primary tumors, the precise pathologic diagnosis of primary adenocarcinoma of the seminal vesicle can only be made if the tumor is located within the seminal vesicle and there is no concomitant tumor in any of the adjacent organs including the prostate, bladder or colon. Histologically, the tumor should have the architectural features of adenocarcinoma, with a papillary or sheet-like growth pattern, mucinous differentiation and carcinoma in situ in the adjacent epithelium lining the seminal vesicle. Immunohistochemistry should demonstrate cytoplasmic reactivity for carcinoembryonic antigen but absence of staining for PSA and prostatic acid phosphatase. The main reason for setting these criteria is that, in cases of locally advanced and high-grade tumors, it may be exceedingly difficult to determine the precise site of origin of the tumor, and tumor cells may appear hobnail, polygonal or columnar with clear cytoplasm.[3] Slayter et al. proposed stratification of the primary adenocarcinoma of the seminal vesicles into three groups: in situ, invasive without desmoplasia and invasive with desmoplasia.[4]

Secondary involvement of the seminal vesicles is usually caused by contiguous spread of tumors from the adjacent organs, and occasionally by metastatic spread. The tumors likely to spread to the seminal vesicles originate from the prostate, bladder and rectum (in decreasing order of frequency). Spread of prostatic adenocarcinoma to the seminal vesicle is the most frequent occurrence. Even in cases of presumed localized adenocarcinoma of the prostate, seminal vesicle involvement is found in up to 12% of radical prostatectomy specimens.

There are three patterns of spread of prostatic adenocarcinoma to the seminal vesicle; direct spread along the ejaculatory duct complex into the seminal vesicles, prostatic capsular perforation followed by extension into the peri-prostatic tissues and the seminal vesicles, and spread by isolated deposits.[5]

Bladder tumors can spread to the seminal vesicles if locally advanced, particularly those that arise from the trigone or base of the bladder. Rarely, the seminal vesicles may be involved by the mucosal spread of the carcinoma in situ of the bladder; the usual route of such a spread is via the prostatic urethra, to the prostatic and ejaculatory ducts and subsequently to the seminal vesicles, or by intra-epithelial replacement or pagetoid spread along the basement membrane.[6]

Adenocarcinoma of the rectum can, in a similar way, spread to the seminal vesicles in locally advanced cases. Metastases to the seminal vesicles are rare but a case of metastatic seminoma has been reported in the literature. Besides the above groups of tumors, a variety of soft tissue tumors, consisting of pure stromal elements such as leiomyomas and fibromas, can arise from the seminal vesicles. There is a unique group of tumors, called 'mixed tumors', which can arise from the seminal vesicles; as the name implies, these are composed of a mixture of epithelial and stromal elements. Mixed tumors are extremely rare; only 15 cases of such tumors have been reported in the English literature, variously described as cystadenoma, cystomyoma, low-grade phyllodes tumor, benign mesenchymoma, adenomyosis, and mesonephric hamartoma.

According to the WHO criteria, to qualify for the diagnosis of a mixed seminal vesical tumor the neoplasm must originate from the seminal vesicle. There should be no normal seminal vesicle within the tumor. The tumors should not invade the prostate and immunohistochemistry must be negative for prostate tumor markers (PSA and prostate acid phosphatase) and carcinoembryonic antigen. As cystadenoma did not fulfil the criteria of mixed tumors it was excluded from the WHO list of mixed tumors published in 2004.[7]

The term 'phyllodes tumor' has been applied to a group of tumors with a foliated structure, which are composed of spindle cell stroma and benign epithelial elements. The most common site of origin of these tumors is the breast, followed by the prostate and, rarely, the seminal vesicles. Tumors are categorized either as fibroadenoma, low-grade phyllodes tumor or high-grade phyllodes tumor (also called cystosarcoma phyllodes) according to the density and cytologic features of the stromal component. The presence of infiltrating margins, stromal atypia, increased number of mitotic figures and overgrowth of glands in the stroma are features indicative of malignancy.[8]

Fain et al. have categorized mixed tumors of the seminal vesicles into fibroadenomas, low-grade phyllodes tumor and high-grade phyllode tumors based on cellularity, presence or absence of atypia and the degree of mitotic activity. They proposed that mixed tumors should be categorized as fibroadenomas if the stroma is hypercellular without any atypia or mitosis. Lesions that show hypercellular stroma with atypia but only few mitoses may be regarded as low-grade phyllodes tumor. On the contrary, lesions that show atypical hypercellular stroma and frequent mitosis (1-5 per 10 high-power fields) should be categorized as high-grade phyllodes tumor or cystosarcoma phyllodes. Only two cases of cystosarcoma phyllodes of the seminal vesicles have been reported in the literature.[9,10]

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